Abstract

There is evidence that a reduction in the baroreflex gain contributes to the high blood pressure in SHR. In the present study performed in conscious freely moving rats, we hypothesized that the baroreflex gain was not altered in SHR. To address this question we used two methods for evaluation of the cardiac baroreflex: a) the sequence analysis technique, and 2) the peak of changes in heart rate in response to increase (phenylephrine, PHE) and decrease (sodium nitroprusside, SNP) in mean arterial pressure (MAP) of Wistar (n=15) and SHR (n=21). The sequence analyses were used to evaluate the cardiac baroreflex function over the natural range of variation of arterial pressure, without any pharmacological tools. Considering that the sequence analyses are restricted to a narrow range of arterial pressure variability, we also evaluated the maximal bradycardic response (peak) to pressor response to PHE (i.v.) as well the maximal tachycardic response (peak) to fall in pressure in response to SNP (i.v). All experimental protocols were performed in conscious freely moving rats, previously anesthetized for catheterization of the femoral artery (arterial pressure recordings) and vein (i.v. injections), which were approved by the institutional ethical committee (#187/2011). The peak of reflex bradycardia in SHR in response to PHE was evaluated during the normalization of the MAP by continuous infusion of SNP (from 140 ± 2 to 101 ± 1 mmHg). The data from the sequence analyses show that the slopes of these sequences in both groups were similar (1.89 ± 0.2 vs 2.03 ± 0.2 ms mmHg−1), while the data from changes in MAP in response to PHE (49 ± 4 vs 39 ± 2 mmHg) show that the peak of bradycardic response in SHR was similar to Wistar (−107 ± 13 vs −91 ± 5 bpm). With respect to the reflex tachycardia to fall in MAP in response to SNP (−39 ± 3 vs −51 ± 12 mmHg) it was observed that the peak of tachycardia in SHR was also similar to Wistar (+107 ± 7 vs +112 ± 15 bpm). The data of this study, using two different experimental approaches, are showing that the gain of the cardiac baroreflex in SHR is not altered when compared to Wistar rats. We conclude that changes in the autonomic cardiac components of the baroreflex are not contributing to the high level of MAP observed in SHR.Support or Funding InformationFAPESP and CNPq

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